PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LUNG DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Giant cell interstitial pneumonia (hard metal lung disease, cobalt lung).

Hard metal lung disease is a rare form of occupational lung disease that can occur in workers engaged in the manufacture, utilization, or maintenance of tools composed of hard metal [a material composed mainly of tungsten carbide (WC) and cobalt] or diamond-cobalt. Clinically, the condition resembles hypersensitivity pneumonitis, with subacute presentations and possible evolution to pulmonary fibrosis. However, this interstitial lung disease is uniquely characterized by the presence of bizarre ;;cannibalistic'' multinucleated giant cells in the alveoli and the bronchoalveolar lavage. A pathological diagnosis of giant cell interstitial pneumonitis (GIP) is, therefore, specific for hard metal lung disease, even though not all affected subjects exhibit this pathognomonic feature. Cobalt is the critical toxic component causing hard metal lung disease, hence also the term cobalt-lung. Hard metal lung disease is more likely to occur in poorly regulated workplaces, but its occurrence depends mainly on individual susceptibility, rather than on cumulative exposure, so that even young subjects may be affected.

Journal Article↗

Interstitial lung disease in lung cancer: separating disease progression from treatment effects.

Lung cancer often develops in individuals with pre-existing pulmonary and cardiac pathology. Many of these individuals with pre-existing pathology are also at risk of occupational lung disease. New and worsening symptoms can be secondary to pre-existing pathology, progressive cancer or treatment. Pulmonary toxicity, including interstitial lung disease, following radiotherapy and conventional cytotoxic chemotherapy (e.g. cyclophosphamide, bleomycin), has been recognised for many years. Pulmonary toxicity also occurs with the newer classes of cytotoxic agents, including the deoxycytidine analogue gemcitabine. A small percentage (0.88%) of patients treated with the epidermal growth factor receptor tyrosine kinase inhibitor gefitinib have developed interstitial lung disease. This complication has been reported at a higher frequency in Japanese patients than in US patients (1.9% vs 0.34%, respectively) and in those with pre-existing pulmonary fibrosis. This review discusses the difficulties in both recognition and treatment of gefitinib-associated interstitial lung disease. Symptoms are vague, such as dyspnoea, cough and fever and can be difficult to differentiate from progressive disease, co-existing morbidity and new pulmonary pathology. Diagnosis is, therefore, by rigorous investigation to exclude all other differential diagnoses. Treatment, at present, is supportive and includes discontinuation of gefitinib, oxygen supplementation, high-dose corticosteroids and antibacterials.

Antineoplastic Agents↗

Collagen vascular disease-related lung disease: high-resolution computed tomography findings based on the pathologic classification.

Collagen vascular disease (CVD) can cause a variety of lung abnormalities, including usual interstitial pneumonia, nonspecific interstitial pneumonia, organizing pneumonia, diffuse alveolar damage, lymphoid interstitial pneumonia, bronchiectasis, constrictive bronchiolitis, follicular bronchiolitis, alveolar hemorrhage, pulmonary hypertension, and drug-induced lung disease. The frequency of each lung disease is different among underlying CVDs. Although high-resolution computed tomography (HRCT) findings of lung disease are often nonspecific, there are some characteristic HRCT findings for some lung diseases based on pathologic findings.

Adult↗

Previous lung disease and lung cancer risk among women (United States).

OBJECTIVE: The association between previous lung diseases (PLD) and lung cancer risk has not been studied extensively. We conducted a registry-based case-control study to examine the relation between previous lung diseases and lung cancer among women in Missouri. METHODS: Incident cases (n = 676) were identified through the Missouri Cancer Registry for the period 1 January 1993 to 31 January 1994. Controls (n = 700) were selected through drivers' license files and Medicare files. RESULTS: Whether analyzing all respondents or in-person interviews only, elevated effect estimates were noted for several types of PLD. Elevated relative risk estimates were shown for chronic bronchitis (odds ratio [OR] = 1.7; 95% confidence interval [CI] = 1.2-2.3), emphysema (OR = 2.7; 95% CI = 1.8-4.2), pneumonia (OR = 1.6; 95% CI = 1.2-2.0), and for all PLDs combined (OR = 1.5; 95% CI = 1.2-1.9). Analysis of only direct interviews did not show a substantial or consistent pattern of change in relative risk estimates. Because PLDs identified close to the time of cancer diagnosis could conceivably be misdiagnosed, resulting from early lung cancer symptoms, we evaluated the effects on risk estimates of a "latency exclusion" of up to three years. When these exclusions were taken into account, ORs remained statistically significantly elevated only for emphysema. CONCLUSION: When earlier epidemiologic findings and underlying biological and genetic factors are taken into account, an association between PLD and lung cancer is plausible.

Adult↗

Speech breathing in patients with lung disease.

Lung volumes and breathing patterns used during speech differ from those of quiet respiration and may be expected to vary with different types of lung disease. To test this possibility, 41 patients with asthma, emphysema, or sarcoidosis and 16 healthy subjects completed a speech protocol. Volumes, times, and flow rates were recorded during conversation and during a counting task. A total of 16 measured variables were derived for each breath and analyzed statistically. Alterations in speech breathing were disease and task specific. Discriminant function analysis applied to data from either speech task could correctly classify subjects with more than 50% accuracy, showing that different patterns were significantly disease specific. Compared with healthy subjects during conversation, all patients averaged a more rapid respiratory rate and increased the proportion of time spent on inspiration (Ti/Ttot). During counting, patient groups showed a variety of patterns, most commonly subordinating metabolic need to communication drive and sounding more breathless to observers. Regression analysis was used to determine how strongly changes in measured speech variables related to degree of physiologic impairment. The effect of severity of disease on speech production is distinguishable from the effect of the diagnostic category.

Adult↗

Preexisting lung disease and lung cancer among nonsmoking women.

Preexisting lung disease was examined as a risk factor for lung cancer in a population-based, case-control study of nonsmoking women in Missouri conducted between June 1, 1986, and April 1, 1991. A history of lung disease was reported by approximately 41% of 618 cases and 35% of 1,402 controls (odds ratio (OR) = 1.2; 95% confidence interval (Cl) 1.0-1.5. The risk was more pronounced when next-of-kin interviews were excluded (OR = 1.5). Previous lung disease was significantly related both to adenocarcinoma (OR = 1.4), which accounted for 62% of the cancers, and to all other cell types of lung cancer combined (OR = 1.8). Despite having discontinued smoking for more than 15 years, long-term ex-smokers were at a 2.2-fold risk of lung cancer compared with lifetime nonsmokers. Among lifetime nonsmokers, significant risks were noted for asthma (OR = 2.7) and pneumonia (OR = 1.5). Emphysema (OR = 2.6) and tuberculosis (OR = 2.0) were also significantly related to lung cancer, but only among former smokers. Chronic bronchitis was linked to elevated risks of nonadenocarcinomas only (OR = 2.3). Pleurisy was not reported more frequently by cases than by controls. Approximately 16% of all lung cancers among nonsmoking women could be attributed to previous lung diseases, most notably asthma, pneumonia, emphysema, and tuberculosis.

Adult↗

Lung volumes and expiratory flow limitation during exercise in interstitial lung disease.

Lung volumes were measured at rest and during exercise by an open-circuit N2-washout technique in patients with interstitial lung disease (ILD). Exercise tidal flow-volume (F-V) curves were also compared with maximal F-V curves to investigate whether these patients demonstrated flow limitation. Seven patients underwent 4 min of constant work rate bicycle ergometer exercise at 40, 70, and 90% of their previously determined maximal work rates. End-expiratory lung volume and total lung capacity were measured at rest and near the end of each period of exercise. There was no significant change in end-expiratory lung volume or total lung capacity when resting measurements were compared with measurements at 40, 70, and 90% work rates. During exercise, expiratory flow limitation was evident in four patients who reported stopping exercise because of dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evident. In all patients, the mean ratio of maximal minute ventilation to maximal ventilatory capacity (calculated from maximal F-V curves) was 67%. We conclude that lung volumes during exercise do not significantly differ from those at rest in this population and that patients with ILD may demonstrate expiratory flow limitation during exercise. Furthermore, because most patients with ILD are not breathing near their maximal ventilatory capacity at the end of exercise, we suggest that respiratory mechanics are not the primary cause of their exercise limitation.

Airway Obstruction↗

A new method for investigating regional lung function in children with localized lung disease.

Lung function studies using 13Nitrogen have been used to determine regional and total lung function in 16 children suspected of having localized lung disease amenable to surgery. This method is simple, requires no active co-operation on the part of the child and gives a radiation dosage of about one-third of that for a bronchogram. The studies provided information about the severity and localization of the disease, and in addition, information about the remaining lung areas.

Asthma↗

Association between celiac disease and lung disease.

An association has been suggested between celiac disease and diffuse interstitial lung disease of the hypersensitivity pneumonitis type in several reports from Europe. The present report consists of a study of 18 North American, biopsy-proved celiac patients, who were compared with an equal number of control subjects balanced for age, sex, and smoking. The celiac patients showed no evidence of interstitial lung disease as assessed by chest roentgenograms and pulmonary function tests. However, a history of asthma or chronic cough was present in a higher proportion of the celiac than control subjects. Also the celiac patients showed objective evidence of airway obstruction, as demonstrated by differences between the two groups in FEV1 (P less than 0.05) and Vmax 50% and Vmax 25% (P less than 0.01 and less than 0.05, respectively). These results confirm a recent report questioning whether there is truly a relationship between celiac disease and interstitial lung disease. Nevertheless, our findings suggest an association between celiac disease and airway obstruction.

Antigen-Antibody Complex↗

Mitogenic activity of tracheal effluents from premature infants with chronic lung disease.

Lung injury alters the expression and release of growth factors that disrupt postnatal pulmonary development in newborns and causes chronic lung disease (CLD). The effect of these factors, released into the airways of newborns with CLD, on cell proliferation and collagen production was characterized in vitro. Human fetal lung fibroblast and alveolar-epithelial-like cell lines (FHs 738Lu and A549, respectively) were exposed to tracheal effluents from infants with CLD (mean gestation, 24.7 +/- 0.9 wk; birth weight, 666 +/- 85 g; postnatal age, 0-62 d). In both cell types, proliferation was assessed by measuring [(3)H]-thymidine uptake; in fibroblasts, collagen production was analyzed by measuring [(3)H]-proline incorporation. The activity of specific growth factors in effluents was determined using anti-growth factor antibodies and the growth factors themselves. Growth factors in tracheal effluents promoted proliferation in a dose-dependent manner and caused up to a 10.2- and 3.1-fold increase in thymidine uptake by fibroblasts and epithelial cells, respectively. Collagen production by fibroblasts increased dose dependently, peaking at 177% of baseline. Antibody against transforming growth factor beta-1 (TGF-beta(1)) inhibited proliferation and the increase in collagen production by 31% (p = 0.01) and 14% (p = 0.045), respectively. Antibody against hepatocyte growth factor (HGF) inhibited proliferation of epithelial cells (25%, p = 0.039). The effects of exogenous TGF-beta(1) on fibroblasts and HGF on epithelial cells resembled those of tracheal effluents. Potent mitogenic and differentiating substances are released into the tracheal effluents of newborns with CLD. TGF-beta(1) may worsen CLD by inducing fibrosis whereas HGF may favor resolution by promoting epithelialization.

Cell Differentiation↗

Oxygen therapy and exercise response in lung disease.

Lung disease affects exercise performance through a number of mechanisms, including hypoxemia, abnormal ventilatory mechanics, abnormal ventilatory muscles, abnormal ventilatory patterns, abnormal right heart function and subjective dyspnea. Supplemental oxygen improves hypoxemia and thus improves exercise impairment resulting from hypoxemia-related reductions in oxygen delivery. Supplemental oxygen also reduces exercise ventilation. This, in turn, reduces ventilatory muscle work, and the concomitant permissive hypercapnia may have beneficial effects at the cellular level. Additionally, in obstructive disease patients, an improved ventilatory pattern may reduce air trapping. Supplemental oxygen may also improve right ventricular dysfunction in patients with underlying right ventricular dysfunction. Finally, supplemental oxygen may reduce dyspnea caused by oxygen-related carotid body activity. Important questions remain. First, is long-term oxygen use of benefit in patients with only exercise hypoxemia? Second, is exercise conditioning possible in patients with exercise hypoxemia? Third, does supplemental oxygen enhance exercise conditioning efforts in those patients with CLD but without exercise hypoxemia? If the answer to this last question is yes, what selection criteria should be used to identify those who would benefit? The answers to all of these questions will have enormous impact on our approach to the optimal management of CLD patients.

Chronic Disease↗

Expression of a human surfactant protein C mutation associated with interstitial lung disease disrupts lung development in transgenic mice.

Surfactant Protein C (SP-C) is a secreted transmembrane protein that is exclusively expressed by alveolar type II epithelial cells of the lung. SP-C associates with surfactant lipids to reduce surface tension within the alveolus, maintaining lung volume at end expiration. Mutations in the gene encoding SP-C (SFTPC) have recently been linked to chronic lung disease in children and adults. The goal of this study was to determine whether a disease-linked mutation in SFTPC causes lung disease in transgenic mice. The SFTPC mutation, designated g.1728 G --> A, results in the deletion of exon4, generating a truncated form of SP-C (SP-C(Deltaexon4)). cDNA encoding SP-C(Deltaexon4) was constitutively expressed in type II epithelial cells of transgenic mice. Viable F0 transgene-positive mice were not generated after two separate rounds of pronuclear injections. Histological analysis of lung tissue harvested from embryonic day 17.5 F0 transgene-positive fetuses revealed that SP-C(Deltaexon4) caused a dose-dependent disruption in branching morphogenesis of the lung associated with epithelial cell cytotoxicity. Transient expression of SP-C(Deltaexon4) in isolated type II epithelial cells or HEK293 cells resulted in incomplete processing of the mutant proprotein, a dose-dependent increase in BiP transcription, trapping of the proprotein in the endoplasmic reticulum, and rapid degradation via a proteasome-dependent pathway. Taken together, these data suggest that the g.1728 G --> A mutation causes misfolding of the SP-C proprotein with subsequent induction of the unfolded protein response and endoplasmic reticulum-associated degradation pathways ultimately resulting in disrupted lung morphogenesis.

Animals↗

Association between initial disease presentation, lung disease outcomes, and survival in patients with cystic fibrosis.

This US study was conducted to determine whether mode of diagnosis and initial disease presentation influence lung disease and survival in patients with cystic fibrosis. The study population included 27,703 patients reported to the 1986-2000 Cystic Fibrosis Foundation Registry. Patients were segregated into four diagnostic categories: meconium ileus (MI), prenatal/neonatal screening (SCREEN), positive family history (FH), and symptoms other than meconium ileus (SYMPTOM). When compared with patients in the SCREEN group, those in the MI or SYMPTOM group were found to have significantly greater risks of shortened survival, Pseudomonas aeruginosa acquisition, and forced expiratory volume in 1 second (FEV(1)) below 70% of predicted. In the SYMPTOM group, the greatest risks of shortened survival, P. aeruginosa acquisition, and FEV(1) <70% occurred for patients presenting with combined respiratory and gastrointestinal symptoms, followed by respiratory or gastrointestinal symptoms alone; the best outcomes were in patients with other presenting features. Additionally, patients with presumably "severe" genotypes (DeltaF508 plus other class I, II, III mutations in both alleles) had greater risks of shortened survival and P. aeruginosa acquisition compared with patients with presumably "mild" genotypes (class IV or V mutations in one or both alleles).

Age of Onset↗

Anti-inflammatory cytokines in cystic fibrosis lung disease.

Lung inflammation plays a pivotal role in the pathogenesis of airway disease in cystic fibrosis (CF). An imbalance between pro- and anti-inflammatory mediators has been observed and a deficiency in the anti-inflammatory response has been proposed, but this concept remains controversial. In the present study, the concentrations of two anti-inflammatory mediators, lipoxin A (LxA4) and Clara cell protein 10 (CC-10), were assessed in bronchoalveolar lavage fluid (BALF) of CF patients with a wide range of endobronchial inflammation and disease controls with neutrophilic inflammation unrelated to CF. No differences were observed in LxA4 BALF concentrations between CF patients and controls with a similar degree of neutrophilic airway inflammation. Concentrations were also similar in CF patients with mild versus more severe airway inflammation. In contrast, CC-10 concentrations were lower in CF patients, but this decrease was limited to patients with more intense airway inflammation. The present data do not support the concept of a primary defect in anti-inflammatory mediators in cystic fibrosis lung disease. Although Clara cell protein concentrations were found to be reduced, these alterations appear to be secondary to neutrophilic airway inflammation rather than due to a primary deficiency.

Adolescent↗

Chronic interstitial lung disease with lung fibrosis in a girl: uncommon sequelae of Epstein-Barr virus infection.

A 12-month-old immunocompetent girl presented with tachypnea, inspiratory crackles, mild hypoxemia, and failure to thrive after an acute Epstein-Barr virus (EBV) infection. The course of acute EBV infection was demonstrated by viral load measurement in plasma and peripheral blood mononuclear cells (PBMC) by using real-time polymerase chain reaction (PCR). EBV DNA was further detected by PCR in bronchoalveolar lavage (BAL) fluid and from a lung-tissue specimen obtained by open-lung biopsy, which indicates the pulmonary involvement of active EBV infection. Histology revealed an uncharacteristic interstitial infiltration and fibrosis. Following topic and systemic treatment with corticosteroids, the child became asymptomatic and showed normal weight gain as well as mental and physical development. Pulmonary parenchymal involvement during the course of primary EBV infection may result in interstitial lung disease and fibrosis not only in immunodeficient, but in immunocompetent children as well. Treatment with combined inhaled and oral steroids seems to be a treatment option in these patients.

Antibodies, Viral↗

Lung epithelial ion transport in neonatal lung disease.

Lung epithelial ion transport promotes salt and water movement across the fetal and neonatal lung epithelium. The mechanism is dependent on basolateral membrane Na-K-ATPase and the apical membrane Cl(-) and Na(+) channels. During fetal life active secretion of Cl(-) and parallel movement of Na(+) across the epithelium into the developing lung lumen induce accumulation of liquid into the future airspaces. Postnatally, however, absorption of fluid from the airspaces must start. Present evidence suggests that activation of Na(+) transport from the lumen into the basolateral direction drives fluid absorption and results in an essentially dry air-filled alveolus. In laboratory animals amiloride, a Na(+) channel blocker, induces respiratory distress and impedes lung fluid clearance. One of the epithelial amiloride-sensitive Na(+) channels, ENaC, is composed of three homologous subunits that differentially respond to glucocorticoid hormone. In newborn infants an increase in pulmonary fluid and a defective Na(+) transport associate with respiratory distress. The ontogeny, subunit composition and function of ENaC along the respiratory tract are currently under investigation. It will be interesting to find out whether the subunit composition and function of lung ENaC respond to the therapy of the critically ill newborn infant.

Animals↗

Action of isoprenaline on the mechanical properties of lungs and airways in healthy people and patients with obstructive lung diseases.

Lung volumes, maximal expiratory flows, pulmonary resistance and static recoil pressure-volume curves were measured before and after inhalation of isoprenaline in four groups of subjects: heqlthy patients with mild and severe chronic bronchitis and asthmatics. The observed changes were qualitatively similar in the four groups. Whereas total lung capacity and dynamic compliance were not influenced, there was an increase in vital capacity (not in healthy subjects and mild bronchitics), in FEV1, in maximal expiratory flows and a decrease in pulmonary resistance. The static recoil pressure-volume relationship was shifted to the left over its ascending part. The effect of isoprenaline tended to be larger in patients. Among the latter, the increase of vital capacity was especially pronounced in the severe bronchitics, whereas the maximal flows increased most in asthmatics. We suggest that the influence of isoprenaline on maximal flows results from a bronchodilation, associated with an increased collapsibility of the central intrathoracic airways, whereas the influence of VC might reflect a delayed onset of small airway closure.

Adult↗

Mean alveolar pressure during constant-flow and constant-pressure inflation of diseased lungs.

INTRODUCTION: An important goal in managing mechanical ventilation is optimizing key variables such as mean alveolar pressure (PA). PURPOSE: Determine the effects of lung mechanics on PA during constant-flow inflation (CFI) and constant-pressure inflation (CPI) in models of nonhomogenous lung disease. METHODS: We postulated a mathematical lung model consisting of 2 parallel lung units with the airways and the chest wall. Analysis was performed for step inputs of inspiratory flow and pressure while maintaining the same tidal volume, respiratory frequency, and positive end-expiratory pressure. The analysis was performed for purely restrictive, purely obstructive, and mixed lung disease. RESULTS: When simulating purely restrictive lung disease, PA was always higher in healthy alveoli than in diseased alveoli, with constant inspiratory flow or constant inspiratory pressure. However, PA in each alveoli was always greater during CPI than during CFI. For purely obstructive lung diseases, PA was always lower in diseased alveoli than in healthy alveoli, with constant inspiratory flow or constant inspiratory pressure. However, PA in each alveoli was always greater during CPI than during CFI. For mixed lung diseases with equal time constants, PA was always higher in diseased alveoli than in healthy alveoli, with constant inspiratory flow or constant inspiratory pressure. However, PA in each alveoli was always the same during CPI as during CFI. CONCLUSIONS: For the same tidal volume, the mean alveolar pressure in different alveoli depends on the type of disease. The difference in mean alveolar pressure between a normal and a diseased alveolus depends on the difference in time constant between those alveoli, regardless of the mode of ventilation.

Airway Resistance↗